بررسی اثر بتا‌‌آسارون بر غلظت فاکتور نکروز توموری- آلفا در مدل موش صحرایی آلزایمری‌شده

آسیب‌شناسی درمانگاهی دامپزشکی

مقاله 2، دوره 15، 1 (57) بهار، اردیبهشت 1400، صفحه 1-12   

نوع مقاله: مقاله علمی پژوهشی

شناسه دیجیتال (DOI): 10.30495/jvcp.2020.670353

نویسندگان

گلشید ساکی¹؛ اکرم عیدی^{* 2}؛ سید پژمان مرتضوی³؛ اکبر وحدتی⁴؛ نگار پناهی⁵

¹دانش‌آموخته دکترای تخصصی گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات فارس، دانشگاه آزاد اسلامی، فارس، ایران؛ دانش‌آموخته دکترای تخصصی گروه زیست شناسی، دانشکده علوم، کشاورزی و فن‌آوری‌های نوین، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

²استاد گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.

³دانشیار گروه پاتولوژی، دانشکده علوم تخصصی دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.

⁴استاد گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات فارس، دانشگاه آزاد اسلامی، فارس، ایران؛ استاد گروه زیست شناسی، دانشکده علوم، کشاورزی و فن‌آوری‌های نوین، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

⁵استادیار گروه علوم پایه، دانشکده علوم تخصصی دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.

چکیده

بتا­آسارون ماده موثره گیاه Acorus tatarinowii Schott می­باشد که قادر به عبور از سد خونی مغز بوده و بر سیستم اعصاب مرکزی تاثیر می­گذارد. در تحقیق حاضر اثر بتا­آسارون بر غلظت فاکتور نکروز توموری-­ آلفا (TNF-α) به­دنبال دریافت بتا­آمیلویید در مغز موش­های صحرایی نر بالغ مورد بررسی قرار گرفت. موش­های صحرایی نر بالغ به­صورت تصادفی به 9 گروه 6 تایی تقسیم شدند: گروه کنترل سالم، گروه شاهد جراحی، گروه­های دریافت­کننده بتا­آسارون (5/12، 25 و 50 میلی­گرم بر کیلوگرم وزن بدن به­صورت خوراکی به مدت 50 روز)، گروه کنترل آلزایمری (دریافت­کننده یک دوز 4 میکرولیتری بتا­آمیلویید 42-1 به­صورت تزریق دو­طرفه در هیپوکامپ) و گروه­های آلزایمری­شده و دریافت­کننده بتا­آسارون (تیمار دوزهای 5/12، 25 و 50 میلی­گرم بر کیلوگرم وزن بدن بتا­آسارون به­صورت خوراکی به مدت 30 روز و بعد از دریافت بتا­آمیلویید، ادامه تیمار با بتا­آسارون به مدت 3 هفته). در پایان آزمایش حیوانات کشته شدند و غلظت TNF-α در هموژنات مغز اندازه­گیری گردید. تیمار بتا­آسارون در دوزهای 25 و 50 میلی­گرم بر کیلوگرم وزن بدن، موجب کاهش غلظت TNF-α در موش­های صحرایی آلزایمری­شده گردید(001/0p <). با توجه به یافته­های حاصل از این مطالعه می­توان نتیجه­گیری کرد که بتا­آسارون در محافظت در برابر التهاب حاصل از دریافت بتا­آمیلویید در بافت مغز موش صحرایی نقش موثری ایفا می­کند.

کلیدواژه‌ها

بتا‌آسارون؛ بتا‌آمیلویید؛ فاکتور نکروز توموری-‌ آلفا؛ موش صحرایی؛ آلزایمر

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